SURGERY_1.4 Small Intestine (Lecture).docx

I.4a – Small Intestine (Lecture-based) Dr. Bibera July 6, 2013 ANATOMY  Small Intestine is the longest organ extending from the duodenal cap to the ileocecal valve  Longest organ and 80% of the GIT  Measures 4 to 6 m  Historically, believed to have 2 key functions:  Absorption of nutrients  Maintain balance between absorption and secretion of H2O and electrolytes  Serves as the largest and most complex endocrine gland  Important immunologic defense barrier DUODENUM  Duodenal cap/bulb  Invested by mesentery  Measures 5cm and closely related to the pancreas  Site of over 90% of ulcer usually penetrating and eroding the gastroduodenal artery  Posteriorly related are pancreas, portal vein and common bile duct  Descending portion  Measures 10cm coursing posteriorly and caudally at L1 and L2  Closely attached to the pancreas  Overlying the Gerota’s fascia and medial to IVC  Midpoint of the 2nd portion enters papilla  Transverse portion  Entirely retroperitoneal in location  Attached to the uncinate process of the pancreas  Wedged between the SMA and aorta  Fourth portion  Turns superiorly & obliquely from the SMA along the border of the pancreas  Bends sharply  Passes superiorly and obliquely from the SMA along the border of the pancreas to reach the ligament of Trietz JEJANUM & ILEUM  Extends from the ligament of Trietz to the ileocecal valve (valve of Gaerlach)  Measuring about 250 cm to 270 cm JEJUNUM  Widest portion of SI in volume  Measures 100-110cm in length (40%)  Diameter progressively decreases with distance ILEUM  Distal 3/5 which is about 150-160cm in length (60%)  Thin-walled with abundant lymphoid tissues (Peyer’s patches) Table 1. Comparison between Jejunum and Ileum JEJENUM ILEUM Length 100-110 cm 150-160 cm Walls Thicker Thinner Plica Circularis More prominent Less prominent Diameter Wider Narrow Mesenteric fat Thinner Thicker Vasa Recta Longer Shorter Arcades Few Numerous ARTERIAL BLOOD SUPPLY  Duodenum  Hepatic artery o Gastroduodenal artery o Pancreatico-duodenal artery  Superior Mesenteric artery Pat, Suzie, Dale, Lenard, Morrice, Charlie, Gemmy

 Jejenum and Ileum  Superior Mesenteric artery BLOOD SUPPLY FROM SUPERIOR MESENTERIC ARTERY  Jejenum  Vasa recta long and end arteries from short arcades  Vessels not obscured by fatty tissues  Mucosa smooth interrupted by valvulae circulares  Ileum  Shorter and less frequent vasa recta  Numerous arcade  Obscured by fatty tissues VENOUS AND LYMPHATIC DRAINAGE  Venous drainage follows the arteries  Dwell in the distal portion of the Peyer’s patches  Drains from the mucosa  wall  regional lymph nodes  Proceeds to the cisterna chili to the thoracic duct  Provides transport of lipids, immune system and spread of malignancy EXTRINSIC NERVOUS SYSTEM  Parasympathetic fibers from the vagus  provides efferent fibers mediating peristalsis, feeling of nausea, vomiting and distention  Sympathetic fibers travel in the splanchnic area and synapse with the superior ganglia  Inhibits motility and secretion  Mediates pain sensation HISTOLOGY Table 2. Layers of the Small Intestine SEROSA  visceral peritoneum  single layer of mesothelium MUSCULARIS  Thin, outer longitudinal muscle and thicker circular muscle  between layers are the Ganglion of Auerbach SUBMUCOSA  strongest layer with fibroelastic tissue  contains networks of lymphatics, blood vessels and Meissner’s ganglion MUCUS  consisting of: MEMBRANE  muscularis mucosa  lamina propria  epithelium PHYSIOLOGY DIGESTION AND ABSORPTION  main role  Epithelium responsible for the absorption and secretion  Mechanism is either by:  Active transport- transfer of solutes in the absence of electrochemical gradients  Passive transport- diffusion or convection with existing gradient

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WATER AND ELECTROLYTE ABSORPTION AND SECRETION Fluid going in: 8-10 liters per day Absorption by SI: 7500ml Diffusion, Osmosis, Active Transport Absorption by Colon: 1500 ml Most are absorbed by the small bowel by simple diffusion, osmosis and active transport Page 1 of 11

 500ml to 1500ml  Electrolytes absorbed and water-soluble vitamins by active transport  Fat-soluble vitamins absorbed with the micelle

Figure 2. Water and Electrolyte Absorption and Secretion

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Table 3. Regulation of Intestinal Absorption and Secretion Agents that Agents that STIMULATE STIMULATE ABSORPTION SECRETION (or inhibit secretion of (or inhibit absorption water) of water) Aldosterone  Secretin Glucocorticoids  Bradykinin Angiotensin  Prostaglandins Norepinephrine  Acetylcholine Epinephrine  Atrial natriuretic factor Dopamine  Vasopressin Somatostatin  Vasoactive intestinal Neuropeptide Y peptide Peptide YY  Bombesin Enkephalin  Substance P  Serotonin  Neurotensin  Histamine

 Digestion continue in the SI and split further the dipeptides, tripeptides and longer proteins  These pass the cellular membrane and goes to portal circulation  80-90% complete in the jejunum

Figure 4. Protein Digestion FAT ABSORPTION  Adult consumes 60g to 100g/d (40%)  Triglycerides (glycerol, FFA and phospholipids cholesterol and lecithin)  Digestion occurs in the small bowel  Broken down into free fatty acids and 2 monoglycerides  Emulsification facilitated by bile making it soluble to water  Micelles formation with hydrophilic outer portion make absorption easily by diffusion

ELECTROLYTE ABSORPTION  Nutrient-coupled Na  Na/H+ exchange  Na channels on the basolateral membrane mediated by Na/K+ ATPase

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CARBOHYDRATE ABSORPTION Adult consumes about 400 gm 60% starch, 30% sucrose, 10% lactose 20% of starch is amylose broken down to maltotriose and maltose Brush borders of SI contain enzymes Absorption of monosaccharides by active transport

Figure 3. Carbohydrate Digestion PROTEIN ABSORPTION  Protein breakdown initiated in the stomach (15%) by trypsin into simple amino acids

1.4a – Small Intestine (Lecture)

Figure 5. Fat Digestion VITAMIN AND MINERAL ABSORPTION  Vitamin B12 (cobalamin) malabsorption can result from a variety of surgical manipulations.  water-soluble vitamins for which specific carriermediated transport processes have been characterized include :  ascorbic acid, folate, thiamine, riboflavin, pantothenic acid, and biotin  Fat-soluble vitamins A, D, and E appear to be absorbed through passive diffusion.  Vitamin K appears to be absorbed through both passive diffusion and carrier-mediated uptake. BARRIER AND IMMUNE FUNCTION  Epithelium limits penetration of harmful substances: zonula occludens, zonula adherens and desmosomes  Immune system of mucosa  Bacteria ingested with the nutrients  Presented to APC by M cells, IgA, IgM  Production of defenses by GALT, IgA, mucins and defensins MOTILITY  Contractions of the muscularis mucosa contribute to mucosal or villus motility, but not to peristalsis.  Propulsion of food Page 2 of 11

 Mediated by pacesetter in the muscularis mucosa known as interstitial cells of Cajal and external neurohormonal signals PATTERNS OF MUSCULARIS PROPRIA  ascending excitation  descending inhibition DIFFERENT TYPES OF CONTRACTION  Fed or postprandial pattern  begins within 10 to 20 minutes of meal ingestion and abates 4 to 6 hours afterward  Rhythmic segmentations  pressure waves traveling only short distances also are observed  The FASTING PATTHER  Or interdigestive motor cycle (IDMC)  consists of three phases: Phase I motor quiescence Phase II seemingly disorganized pressure waves occurring at submaximal rates Phase III sustained pressure waves occurring at maximal rates  This pattern is hypothesized to expel residual debris and bacteria from the small intestine.  The median duration of theIDMC ranges from 90 to 120 minutes ENDOCRINE FUNCTION  Rich source of regulatory peptides  Released as response to stimuli  Exerts action locally as paracrine or distally as hormone  Peptides used in practice (Secretin, Ocreotide, Cholecystokinin) Table 4. Representative Regulatory Peptides HORMONE SOURCE ACTIONS SomatoD cell  inhibits gastrointestinal statin secretion, motility and splanchnic perfusion Secretin S cell  Stimulate exocrine pancreatic secretion; stimulate intestinal secretion CholeI cell  Stimulate exocrine cystokinin pancreatic secretion; stimulate gallbladder emptying; inhibit sphincter of Oddi contraction Motilin M cell  Stimulates intestinal motility Peptide YY L Cell  Inhibits intestinal motility and secretion GlucagonL cell  Stimulate intestinal like epithelium proliferation peptide 2 NeuroN cell  Stimulate pancreatic and tensin biliary secretion; inhibits small bowel motility; stimulate intestinal mucosal growth SMALL BOWEL OBSTRUCTION  Approach to intestinal obstruction parallel to the development of safe surgery  Frederick Treves in 1884, laid the foundation of recognition and management of SBO  In 1912, recognized the value of IV fluid resuscitation  In 1920, radiograph used for diagnosis  In 1925, decompression recognized to provide relief  Principles of management established i.e. rapid IVF and electrolyte resuscitation, decompression and early operation, before antibiotic, TPN and monitoring  Definition: When there is failure of contents to pass distally.

1.4a – Small Intestine (Lecture)

TERMINOLOGY AND CLASSIFICATION  Mechanical obstruction  Inability of the luminal contents to pass thorough due to blockade  Neurogenic or Functional obstruction  Passage is prevented due to disturbance of gut motility  Ileus- if it involves the small intestine  Pseudo-obstruction- if it involves the large intestine PRESENCE OR ABSENCE OF VASCULAR INVOLVEMENT  Simple obstruction- there is no compromise of blood flow  Partial or incomplete o Narrowed lumen but permits passage of contents o Dx: radiographic exam o Tx: not necessarily operative  Complete o Lumen totally occluded and prevents passage of contents distally  Strangulated obstruction- there is compromise of blood flow, necrosis and gangrene imminent even if obstruction is partial or complete INTRALUMINAL  Foreign bodies  Barium inspissations (colon)  Bezoar  Inspissated feces  Gallstone  Parasites  Other (swallowed objects, enterocolitis)  Intussuception  Polypoidexophytic lesion INTRAMURAL Congenital  Atresia, stricture or stenosis  Web  Intestinal duplication  Meckel’s Diverticulum Neoplasms Inflammatory process  Crohn’s disease’  Diverticulitis  Chronic intestinal ischemia  Postischemic stricture  Radiation enteritis  Medication induced (NSAIDS, KCl tablets) EXTRINSIC Adhesions Congenital  Laddormeckel’s bands  Postoperative  Postinflammatory Hernias  External (inguinal, femoral)  Internal Volvulus External mass effect  Abscess  Annular pancreas  Carcinomatosis  Endometriosis  Pregnancy  Pancreatic pseudocyst SITE OR SEGMENT INVOLVED  Proximal or high obstruction  includes the pylorus, duodenum and proximal jejunum  Intermediate  from the mid-jejunum to mid-ileum  Distal obstruction  from distal ileum to proximal colon  Low obstruction  beyond the transverse colon  Open obstruction

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 flow of contents blocked but proximal decompression possible  loss of gastric, pancreatic and biliary secretions  metabolic alkalosis develops  Closed-loop obstruction  both the inflow and outflow are blocked, e.g. torsion, volvulus, hernia  Rapid increased pressure, hasten infection, gangrene and perforation. SYMPTOMS AND SIGNS OF BOWEL OBSTRUCTION Symptom or sign PAIN

VOMITING

Proximal Small Bowel  Intermittent, intense, colicky, often relieved by vomiting  Large volumes, billous and frequent

TENDERNES S

 Epigastric, or periumbilical; quite mild unless strangulation is present DISTENTION  Absent OBSTIPATIO N

 May not be present

Distal Bowel  Intermittent to constant  Low volume and frequency, progressively feculent with time  Diffuse and progressive

 Moderate to marked  present

Symptom or sign PAIN

Small Bowel Colon and (Closed Loop) Rectum  Progressive,  Continuous intermittent to constant, rapidly worsens VOMITING  May be  Intermittent, not prominent prominent, (reflex) feculent when present TENDERNES  Diffuse,  Diffuse S progressive DISTENTION  Often absent  Marked OBSTIPATIO N            

 May not be present

 Present

COMMON ETIOLOGIES Adhesions- most common Neoplasms Primary small bowel neoplasms Secondary small bowel cancer (melanoma-derived metastasis) Local invasion by intra-abdominal malignancy (desmoids tumors) Carcinomatosis Hernia External (inguinal and femoral) Internal (following Roux-en-Y gastric bypass surgery) Chron’s disease Volvulus Intussusceptions

Figure 6.Common causes of small bowel obstruction in industrialized countries. PATHOPHYSIOLOGY  Motility  Fluid and gas accumulation elicit myoelectric proximal and distal functions  Intense period of peristalsis, above and below  Protective mechanism – receptive relaxation  Diminution of activity and ineffective contraction due to fatigue causing distension  Mediated by neurohormones, toxins, luminal and conditions  Intestinal Gas  Mostly from swallowed air in 80%  Consisting mostly of nitrogen and small amounts of other gasesas oxygen, carbon dioxide, etc  Fluid/Electrolytes Non-obstructed:  Mostly from swallowed air from 80%  Consisting mostly of nitrogen and small amounts of other gases as oxygen, carbon dioxide, etc  Absorption of fluid not impaired In SBO:  Increasing pressure and distention>20cm H2O inhibits absorption and stimulates secretion of salts and water into the lumen  Release of pro-secretory and anti-anbsorptive hormones as vasoactive inhibitory peptide and prostaglandins  Flora Non-obstructed:  Chyme entering the duodenum nearly sterile  Small number of aerobic gram +/- and anaerobes in the distal portion  Normal flora responsible for the secretions and motility of the bowel, short chain FA, bile acid metabolism, fat-soluble vitamins and gas formations In SBO:  Stasis favors change of flora and overgrowth  Alters motility, transport properties, perfusion, and lymph flow  Endotoxin production stimulates secretions and altered response to inflammation and nitric oxide  Intestinal Blood Flow  Increased flow as initial response  Hydrostatic and osmotic pressure favor flow of ECF to lumen  Perfusion is compromised  Bacterial invasion causes edema of fluid  Wall ischemia and necrosis  Partial bowel obstruction  Part of the lumen is obstructed  Allows passage of gas and fluid  Less likely to develop strangulation  Closed-loop obstruction  Dangerous form  Proximal and distal obstruction of a segment  Rapid rise of luminal pressure and gangrene        

1.4a – Small Intestine (Lecture)

CLINICAL MANIFESTATIONS Colicky abdominal pain Nausea and vomiting Abdominal distension Failure to pass flatus and feces Fever Tachycardia and hypotension Distended peristaltic waves Hyperactive bowel sounds Page 4 of 11

 Mild tenderness with or without mass  Examination to include groin and rectal

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DIAGNOSIS  Focused on the following:  Mechanical vs ileus  What is the etiology  Partial vs complete obstruction  Simple or strangulated

Collapsed distal ileum Doppler ultrasound (Ogata, et al) Akinetic bowel Presence of peritoneal fluid Bull’s eye sign

COMPLICATIONS AND SYSTEMIC EFFECTS  Rapid onset of manifestations due to obstruction  Gangrene and necrosis occurs  Toxins from bacterial overgrowth released to systemic circulation  Septicemia and shock

Doughnut Sign

IMAGING STUDIES Radiograph Imaging  sensitivity of 70-80%  To confirm the presence of obstruction  To determine the site of obstruction  To determine the etiology MANAGEMENT PLAIN FILM OF THE ABDOMEN  TRIAD of findings:  Dilated Bowel Loops o >3cm if the small intestine involved o >8-10cm of the cecal diameter and 4-5cm o If the colon is obstructed  Step-ladder Sign or Air Fluid levels  Paucity of air in the colon  Pneumoperitoneum (not sure kung under itong above. Labong numbering ni Doc) A. Contrast Studies  With the use of barium, gastrografin or hypaque  Specific site of obstruction  Usually unnecessary in SBO  Helpful in colonic obstruction  Recurrent obstruction  Low grade mechanical SBO Bird’s Beak or Ace of Spade in Volvulus

Apple-core appearance in Colon CA

NON-OPERATIVE TREATMENT For non-complicated SBO CONTRAST STUDIES IN PARTIAL SBO  Passage of contrast medium into the colon after 8 hours  Resolution in 19%  Landescasper in 4 yr study  Non-operative recurrence 53%  Operative recurrence 29% CONTRAST STUDIES IN COMPLETE SBO  Fleshner Study found 45% success rate OPERATIVE MANAGEMENT  Lysis of adhesions  By-pass procedure  Decompression ileostomy or colostomy  Bowel resection  Reduction and hernia repair  Drainage of abscess  Questions regarding viability 1. Color 2. Peristalsis 3. Pulsations 4. Doppler studies 5. Fluorescein dyes 6. “Second look” MANAGEMENT Objective:  To correct the existing fluid/electrolyte imbalance  To treat the underlying cause of obstruction Questions to be asked: 1. Severity of the pain 2. Rapidity of onset and development 3. Fluid and electrolyte imbalance 4. Determine if complete or partial obstruction 5. Determine presence of strangulation

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CT Scan SB distended > 25 mm, detects transition zone Ability to distinguish complete or partial obstruction Nature of cause of obstruction or location Determine additional pathologic conditions e.g. tumors, abscess, IBD  Strangulation late stage, intestinal wall  Limited use in partial SBO

C. Ultrasound  Detects bowel diameter >25mm 1.4a – Small Intestine (Lecture)

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TREATMENT Restriction of oral feedings Correction of fluid/electrolyte imbalance Decompression Antibiotics

SURGICAL  Determine if surgical intervention is necessary like:  Rapid progression of symptoms  Peritoneal manifestations  Failure to resolve in 24 to 48 hours  Complete obstruction Page 5 of 11

SPECIFIC TYPES OF SMALL BOWEL OBSTRUCTION ADHESIONS  Comprises about 50% of all SBO  Occurs about 5% of all patients who had history of laparotomy esp. pelvic operations  Spontaneously resolves in 80% of cases if obstruction is partial  Foreign body reaction found in pathologic studies of fibrous adhesions  Prevention includes:  Removal of foreign body as: sponge, starch or debris  Good surgical technique: gentle tissue handling, unnecessary dissection and serosal trauma  Choice of suture material  Application of tissue plasminogen activator  Use of omentum around site of surgery

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HERNIA Ranks 2nd cause of SBO Femoral hernia Internal herniation Rrichter’s hernia  Special type GALLSTONE ILEUS Escape of gallstone >2.5cm from fistulous tract between GB and duodenum Occurs in 6/1000 cases SBO radiologic appearance:  Stone lodge in the area of RLQ, ileocecal region  Aerobilia- air in the biliary tree  Recurrence rate of 5-10%  Elective biliary surgery

Figure 7. Aerobilia INTUSSUSCEPTION  Occurs in about 5% among adults  Associated with other conditions as tumors, diverticulum, adenitis  Occurs post-operatively:  Suture lines 20%  Adhesions 30%  Internal tubes 50%  Types:  Enteric  Ileocolic  Ileocecal  Colonic  Diagnosis  Currant jelly stool  Dance sign  Sausage shaped soft tissue  Coil-spring sign on barium enema  Bull’s eye or dough nut sign on ultrasound VOLVULUS  loop of bowel twists 180 degrees around its axis  involves the sigmoid (65%), cecum, transverse colon  Chilaiditi syndrome – redundant between the liver and the diaphragm form of a closed loop type of obstruction  Diagnosis Xray findings of: 1.4a – Small Intestine (Lecture)

1. Bent inner tube sign 2. Ace of spade 3. Bird’s beak  Management:  Endoscopic decompression - 85% to 90% effective with 60% recurrence  Planned resection  Colostomy  Fixation INFLAMMATION OF THE SMALL INTESTINE CROHN’S DISEASE  1932:CrohnGinzburg and Oppenheimer reported on regional ileitis  First termed as “terminal Ileitis”  Cure comes with complete resection  Recurrence - due to incomplete resection  INCIDENCE : Young adults (2nd to 3rd decade of life)

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CLASSIFICATION (AS TO LOCATION) Ileum: 75% Small intestine ONLY: 15 -30% Ileum and colon: 40 -60% Colon ONLY: 5 -30% Anorectal: 5-10%

ETIOLOGY  Remains a mystery \m/  Environmental  Genetic  first degree relatives high risk of Crohn’s  Findings of IBD 1 chr 16  Microbial  M. paratuberculosis, Chlamydia, Reovirus, Pseudomonas  Immunologic  defective immune regulatory mechanism or protracted response to flora derived antigens PATHOLOGY A. GROSS APPEARANCE  Thickened wall with violaceous appearance of the serosa  Messenteric fat encroaches with anti-messenteric portion usually thickened, edematous and with enlarged nodes “fattening of the bowels” and pathognomonic  Apthous ulcers, 3mm  Transmural inflammation causing stricture, abscess, fistula and perforation  Skip areas of normal bowel  Narrowing of the lumen with mucosal ulceration, rake ulcer with intervening raised mucosa (cobblestone appearance) B. MICROSCOPIC  Ulcerations  Marked fibrosis  Lymphangiectasia  Nodular hyperplasia  Non-caseating necrosis in 70% of cases in any layer and LN CLINICAL MANIFESTATIONS Abdominal Pain or mimics appendicitis Loss of appetite Weight loss Diarrhea, malabsorption and anemia Specific manifestations:  Genitourinary – due to endovesical fistula or hydronephrosis  Fistula formation  Perianal disease or fistula-in-ano  Gynecologic as rectovaginal fistula  Gallbladder disease  Extraintestinal Manifestations  Dermatologic     

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o Erythema nodosum o Pyoderma gangrenosum  Rheumatologic o Peripheral arthritis o Ankylosing spondylitis DIAGNOSIS  Based on history and physical exam e.g. unusual fistula-in-ano  Intra op findings  Small bowel series:  Thickened mucosal folds – “Thumb printing”  Cobblestone appearance of the mucosa  String sign  Fistulous tract with other organs or small intestine  pANCA determination TREATMENT  Medical  palliation than cure is the objective  Control of diarrhea with cholysteramin  Care of the perianal disease  Antibiotic coverage: Sulfasalazine  Corticosteroids  Immunosuppressive agents  Anti TNF (Infliximab) for resistant causes  Surgical Intervention  Acute onset of severe disease: Colitis -/+ Toxic megacolon  Failure of medical therapy  Recurrence of symptoms with tapering of steroids  Drug induced complications  Complications of Crohn’s Disease 1. Bowel obstruction-most common 2. Perforation with abscess formation - rare 3. Fistula formation 4. Hemorrhage 5. Malignancy  PROCEDURES 1. Resection as ileoascending colostomy or segmental resection with primary anastomoses 2. Stricturoplasty 3. Others as bY-pass operation RESULTS OR OUTCOME  Overall complications 15-30% as abscess, leakage and wound infection  Recurrence:  Endoscopy: 79% after 1yr and 85% after 3 years  Clinical recurrence about 33% after 5 years from operation  Reoperation after 5 years common DIVERTICULAR DISEASE OF THE SMALL BOWEL  Uncommon clinical entity and usually discovered when looking for other diseases  Varies with anatomic location  Autopsy series have the highest incidence 9-20%  ERCP findings about 2-5% Classifications  Congenital  true diverticulum with protrusion of full thickness of the wall of SI  Acquired  mucosa, submucosa with lack of muscle DUODENAL DIVERTICULUM  Vast majority are congenital  If acquired it is located at the mesenteric side 2nd portion of the duodenum near the exit of the biliary and pancreatic ducts  Incidental findings on EGD or barium swallow with small bowel follow through 1.4a – Small Intestine (Lecture)

 Difficult to treat due to its relationship with other organs and vascular areas MANIFESTATIONS  Biliary in nature as gallstones, cholangitis, and jaundice  Pancreatitis  Diverticulitis and perforation which maybe secondary to instrumentation DIAGNOSIS  EGD, ERCP  UGI series with small bowel follow through  Contrast CT scan in cases of perforation TREATMENT  Usually no treatment necessary in asymptomatic cases  Prophylactic removal is not indicated due to high mortality  Surgical intervention necessary in the presence of perforation, diverticulitis and hemorrhage  Primary excision if the biliary and pancreatic ducts not involved  Closure if the defect is small – invert, tie, excise then close  Serosal patch  Roux-en-Y duodenojejunostomy  In the presence of perforation extensive edema:  Duodenal diverticulization i.e. gastrojejunostomy, closure of the pylorus, repair of the perforation and tube duodenostomy  If there is hemorrhage (erosion of the arcade)  Angiographic embolization  Surgical suture and repair  Endoscopic management destined to fail JEJUNAL DYSKINESIA  A specific intestinal pseudoobstruction characterized by intermittent partial bowel obstruction  Have significant relationship to complications of cholangitis, pancreatic and stone disease JEJUNAL DIVERTICULA  Symptoms secondary to:  Myenteric dysfunction: o Chronic abdominal pain o Early satiety o Diarrhea o Malabsorption with development of vitB12 deficiency and anemia  Perforation, hemorrhage and obstruction  Both types are asymptomatic  Symptomatic in infection, perforation, hemorrhage, and obstruction. TWO TYPES  Congenital  Acquired  usually increasing incidence with age; false diverticula where part of the mucosa or submucosa protrude thru the muscular wall

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DIAGNOSIS UGI series with small bowel follow through Enteroclysis Capsule with wireless endoscopy CTscan in cases of diverticulitis and perforation Angiography Technetium 99 scan

TREATMENT  None is asymptomatic  Resection:  Multiple diverticulae  Perforation Page 7 of 11

 Diverticulitis  Bleeding MECKEL’S DIVERTICULUM  17th century- diverticula was observed as content of a hernia  1672 - Lavater  1701 - Mercy  1770 - Littre’s Hernia  1808 -Johann Friend Meckel discovered that it is a remnant or duct between the intestinal tract and yolk sac  1898 - Kulter described as a case of intusseption involving Meckel diverticulum  1904 - Salzer noted gastric mucosa and ulcer of the ulcer of the adjacent ileum INCIDENCE  In autopsy series the incidence is 0.3-2.5%  Soderlund noted 3.2% of patients who had appendectomy  Common among children 2 years old  M:F 2:1  Incidental findings in adults RULE OF TWO:  2% of general population  2 years old  2 feet from ileocecal valve  2:1 M:F ratio  2 of the most common ectopic tissues  2most common complications: Bleeding and ulceration ETIOLOGY  Partial or complete failure of the omphalomesentericduct to obliterate giving rise to the ff:  Meckel’s Diverticulum  Mesodiverticulum band  Opthalomesenteric fistula  Enterocyst

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PATHOLOGY Length varies from 1-26 cm (2-5cm) Location 10-150cm from the ileocecal valve Soderlund, 1959: Children 40 cm, adult 50 cm Associated with congenital anomalies as exomphalos, atresias, anomalies of the CNS and CVS

MICROSCOPIC  Heterotropic mucosa in 60%: gastric 60%, pancreaticacini second, colonic, endometriosis and hepatobiliary CLINICAL MANIFESTATIONS  Complications in 4% of patients, 50% asymptomatic diverticulamoccu in 10 yr old or younger  Certainty of diagnosis is made during the operation 1. Hemorrhage  40-50% due to peptic ulceration described as bright red or maroon red in 47-57%, tarry stool 7% 2. Obstruction, volvulus, intussusceptions, entrapment 3. Inflammation or Diverticulitis in 20%  Mimics acute appendicitis  Reason to look for if the appendix is normal  Perforate and causes peritonitis 4. Umbilical fistula  Ileal contents ooze thru the umbilicus 5. Littre’s hernia  Inguinal hernia 50%  Umbilical 20%  Femoral 20% 1.4a – Small Intestine (Lecture)

 Incisional 10% 6. Neoplasm  Weinstein, 1963 in 106 cases  Benign 26%  Malignant 80% o Sarcoma 35% o AdenoCA 16% o Carcinoid 29% DIAGNOSIS  CT Scan: not clinically useful  Use of contrast studies as fistulogram  Technetium scan- (Jewett, 1970) if the diverticulum contains gastric mucosa the accuracy is 90% in younger but 2 cm and attached by bands NEOPLASMS OF THE SMALL BOWEL  Rare e through the GIT comprise 40% of all neoplasms  Incidence is 1-3% Reasons why it is rarely involved: 1. Rapid transit of contents ½-2 hrs 2. Local immune system IgA 3. Alkalinity prevents mucosal injury 4. Absence of bacteria prevents genetic alterations 5. Presence of mucosal enzymes benzyopyrene hydroxylase detoxifying the effects of benzopyrenes 6. Rapid replication BENIGN Adenoma Lipoma Leiomyoma Hemartroma Hemagioma

PREV. 15% 15% 18% 15% 13%

MALIGNANT Adenocarcinoma Sarcoma* Lyphoma Carcinoid Malignant Carcinoid

PREV. 35-50% 15-20% 10-15% 20-40%

Heterotropic Tissue *GIST- GI Stromal Tumor from interstitial cells of Cajal as leiomyoma or leiomyosarcoma RISK FACTORS Pre-existing condition  Adenomatous polyp  FAP  PeutzJegher’s Syndrome  Crohn’s Disease  Leiomyoma  Celiac Sprue  HIV; H. Pylori; EBV Potential CA  Adenocarcinoma  Leiomyosarcoma (GIST)  Adeno CA/Lymphoma  Lyphoma CLINICAL PRESENTATION MALIGNANT  Absence of pathognomonic signs/symptoms Page 8 of 11

 Usually they are non-specific  Vague complaints lead to errors and delay of diagnosis  Symptomatic usually the ileum is involved  Diagnosis expedited by onset of complications S/Sx Asymptomatic Abdominal Pain Weight Loss Nausea and Vomiting Bleeding Anemia Abdominal Mass

Frequency 6-12% 62-83% 38-55% 23-64% 6-31% 12-38% 5-32% BENIGN

S/Sx Asymptomatic Abdominal Pain Bleeding Anemia Intermittent Obstruction    

Frequency 47-60% 24-50% 29-44% 28-58% 12-28%

DIAGNOSIS Duration varies from weeks to months Infrequency of incidence Omission of diagnosis Limited imaging techniques:  Plain X-ray  Rarely helpful unless obstruction is present  Useless if presentation is bleeding IMAGING DIAGNOSIS

 CT scan  Identify presence of tumor  Presence of obstruction  Other pathologic conditions  UGIS with small bowel series  Failure of CT to identify tumor  Identify tumor of duodenum – 85-90%  Decrease accuracy with length – 53-87%  Enteroclysis  Using Ba and methycellulose distending the bowel will compromise peristalsis  Able to identify luminal tumor -90%  Small bowel enteroscopy  “Push” enteroscopy with pediatric colonoscopy  Intraoperative colonoscopy  Video capsule endoscopy – 11x26 mm camera w/ battery, light source and transmitter  Angiography and technetium scan BENIGN TUMORS  Accounts for 30-51% of primary tumor  Half of these are asymptomatic  Symptoms consists of: Obstruction, Bleeding, Perforation  Reason enough to have further evaluation ADENOMA  Tubular adenoma  Mostly asymptomatic involving the duodenum  Low malignant potential  Hemorrhage and obstruction if symptomatic  Amendable to polypectomy  Villous adenoma  Distinct malignant potential  Peri-ampullary, bleeding, obstruction and over 3cm size requires removal  Brunner gland adenoma  Hyperplasia of the exocrine gland  Polypoid lesion involving the duodenum LEIOMYOMA  Most common symptomatic tumor

1.4a – Small Intestine (Lecture)

 Arise from interstitial ells of Cajal which over 90% of GIST express CD117 ckit protooncogenes and 70-80% express CD34 (progenitor antigen)  Involving the jejunum and usually solitary  Bleeding results due to outgrowing the vascular supply causing necrosis and ulceration  Presence of 2 mitotic figures/ 50 HPF have a higher risk of local recurrence LIPOMA  More in males than females  Involving the ileum and duodenum  Arise from the adipose tissue of the submucosa and mesenteric fat at the base  No malignant potential  Can be diagnosed by CT scan PEUTZ-JEGHER’S SYNDROME  Inherited disorder  Mucocutaneous melanotic pigmentation circum-orally, palms and soles of feet and GIT polyps and other parts of the body  Polyps are hamartomatous in the jejunum and ileum, colon 50% and stomach in 25%  Few reports of malignant degeneration  Obstruction secondary to intussusceptions HEMANGIOMA  Vascular neoplasm  Related to Osler-Weber-Rendu disease  Bleeding of the lower GIT MALIGNANT NEOPLASMS  Primary malignant tumors:  Adenocarcinoma  Leiomyosarcoma (GIST)  Lymphoma  Carcinoid

    

ADENOCARCINOMA Most common occurring 30-50% of cases Involves duodenum and proximal small bowel – 35% Patients usually in their 6th-7th decade Male predominance Origin  Epithelial cells of the intestinal mucosa  Polyp-to-cancer sequence  Peutz Jegher’s syndrome  Crohn’s disease

DIAGNOSIS  Endoscopic examination  Incidental findings on surgery PRESENTATION  Depend on location of tumor  Weight loss  Abdominal pain  Obstructive jaundice in peri-ampullary lesion  Obstruction if the ileum is involved  Occult blood loss TREATMENT Surgical Management  Resection of the small bowel  Small lesions involving the duodenum  Laparoscopic assisted mid-jejunoileal segment  Right hemicolectomy in terminal ileum  Whipple’s operation 2nd portion of the duodenum Medical Management  Role of chemotherapy and RT is unclear  Response rate using 5 FU is less than 20%  RT no recommended since mucin producing tumor is radio resistant PROGNOSIS AND SURVIVAL  Diagnosed late and nodes are involved

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 Overall 5 yr survival is 5-30% [ (-) nodes 50-70%, (+) nodes 15%] LEIOMYOSARCOMA  Should be reclassified as gastrointestinal stromal tumor or GIST  Arises from connective tissues from muscle blood vessels deep skin and nerve  Origin: Mesodermal component usually the tunica mucosa or muscularis mucosa INCIDENCE  nerve  Sporadic occurrence  Involving 10-20 cases per 1 million population  One of 3-4 cases is malignant

 Malabsorption STAGE I II

SURVIVAL 40-60% 20%

II II II III IV

Negligible

EXTENT Tumor confined to GIT single or multiple Extends from the primary site to lymph node but confined below the diaphragm Tumor penetrated the serosa and adjacent structures Local Nodal Involvement Distal Nodal Involvement Supradiagphragmatic involvement Disseminated both sides of the diaphragm

PRESENTATION  Tendency to grow extra-luminal  Obstruction is late manifestation  Abdominal pain and weight loss  GIT bleeding in 60%  Perforation in 10%

DIAGNOSIS  Contrast study  coarse mucosal folds and sub-mucosal nodules  CT scan  diffuse bowel wall thickening and nodal enlargement

PATHOGENESIS  In the GIT it arises from the interstitial cells of Cajal (ICC)  Part of the ANS with pacemaker function  Responsible in controlling the motility of GIT  Due to gene mutation known as c-kit (CD117 or CD 34) which is a tyrosine kinase

TREATMENT  Surgical  Resection due to obstruction or hemorrhage  Debulking procedure  Staging of the disease  Chemotherapy and RT  Controversial in curative resection in Stage IE and IIE  For advance cases adjuvant therapy indicated

DIAGNOSIS  Barium filled cavity on contrast study  CT scan will show bulky extra – luminal mass TREATMENT  Surgical:  wide en-bloc resection  Extended lymphactenectomy not indicated  Palliative by-pass operating  Chemotherapy and RI  Adriamycin and cyclophosphamide  Radio-resistant PROGNOSIS  Depends on the grade of the tumor which determines prognosis  Presence of mitotic figures/HPF:  Low grade < 10/HPF – 60% to 80%  High grade> 10/HPF - 25mg/24hr  Indium 111 Octreotide tag scan TREATMENT  palliation of symptoms  Cyproheptadine, Methylsergide, histamine antagonist and ocreotide an analogue of somatostatin  hepatic ligation or embolization which is good up to 4 months  hepatic transplant  debulking procedure CHEMOTHERAPY AND RT  Modest response with the use of doxorubicin, 5FU, and streptozocin, 20-30%  No benefit with RT PROGNOSIS  Five year survival of 60%  Patients with carcinoid syndrome is 38 months -END-

This sentence has five words. Here are five more words. Five-word sentences are fine. But several together become monotonous. Listen to what is happening. The writing is getting boring. The sound of it drones. It’s like a stuck record. The ear demands some variety. Now listen. I vary the sentence length, and I create music. Music. The writing sings. It has a pleasant rhythm, a lilt, a harmony. I use short sentences. And I use sentences of medium length. And sometimes, when I am certain the reader is rested, I will engage him with a sentence of considerable length, a sentence that burns with energy and builds with all the impetus of a crescendo, the roll of the drums, the crash of the cymbals–sounds that say listen to this, it is important. 1.4a – Small Intestine (Lecture)

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